System to treat av-conducted ventricular tachyarrhythmia

ABSTRACT

Various aspects of the present subject matter provide devices and methods to treat AV-conducted ventricular tachyarrhythmia (AVCVT). According to various embodiments of the method, an AVCVT is sensed, an IVC-LA fat pad is stimulated when the AVCVT is sensed to block AV conduction, and bradycardia support pacing is provided while the IVC-LA fat pad is stimulated. Other aspects and embodiments are provided herein.

CROSS REFERENCE TO RELATED APPLICATION

This application is a divisional of U.S. application Ser. No.11/099,226, filed Apr. 5, 2005, which is hereby incorporated byreference in its entirety.

TECHNICAL FIELD

This application relates generally to medical devices and, moreparticularly, to systems, devices and methods to treat AV-conductedventricular tachyarrhythmias.

BACKGROUND

A supraventricular tachyarrhythmia (SVT) is an arrhythmia thatoriginates from the supraventricular region, such as the atrium, thesinus node, the AV node or AV junction. Examples of SVT include atrialtachyarrhythmia as well as AV and AV Nodal Reentry Tachyarrhythmias(AVNRT). Atrial tachyarrhythmia includes atrial tachycardias such asatrial flutter, and further includes atrial fibrillation, for example.SVT can be conducted through the AV node, thus resulting in aventricular tachyarrhythmia associated with the SVT. Ventriculartachyarrhythmias triggered by an SVT via conduction through the AV nodeare referred herein as AV-Conducted Ventricular Tachyarrhythmias(AVCVT).

Some SVTs are chronic in nature, whereas others are not chronic. Theduration of these non-chronic SVTs can range from a time period of lessthan a minute to a time period of several days. An example of anon-chronic SVT is paroxysmal atrial tachycardia (PAT), which also maybe referred to as paroxysmal SVT, AVNRT or AV reentry tachycardia. PATis a type of rapid atrial arrhythmia characterized by brief periods ofsudden-onset and often abrupt termination of atrial tachycardia. Thesudden onset of the tachycardia is caused by micro-reentry within the AVnode or macro-reentry between the AV node and a bypass tract, and can beassociated with uncomfortable and annoying symptoms such aslightheadedness, chest pain, palpitations, anxiety, sweating andshortness of breath. An atrial tachycardia can evolve into more seriousarrhythmias like ventricular tachycardia.

Implanting a chronic electrical stimulator, such as a cardiacstimulator, to deliver medical therapy(ies) is known. Examples ofcardiac stimulators include implantable cardiac rhythm management (CRM)devices such as pacemakers, implantable cardiac defibrillators (ICDs),and implantable devices capable of performing both pacing anddefibrillating functions. However, some SVTs, such as PAT, can bedifficult to treat because it typically is not considered to be lethalenough to warrant defibrillation shock treatment or surgical AV nodalablation, which prevents the rapid ventricular heart rate associatedwith the SVT.

SUMMARY

Various aspects of the present subject matter relate to an implantablemedical device. In various embodiments, the device comprises at leastone port, a sensing circuit, a neural stimulation circuit, a pacingcircuit and a controller. Each port is adapted to connect at least onelead that has at least one electrode. The sensing circuit is connectedto the at least one port to sense at least one intrinsic signal for usein determining an AV-Conducted Ventricular Tachyarrhythmia (AVCVT)event. The neural stimulation circuit is connected to the at least oneport to selectively apply a neural stimulation signal to an IVC-LA fatpad. The pacing circuit is connected to the at least one port to providebradycardia support pacing to maintain at least a programmable minimumheart rate. The controller is connected to the sensing circuit, theneural stimulation circuit and the pacing circuit. The controller isadapted to determine the AVCVT event from the at least one intrinsicsignal sensed by the sensing circuit, apply the neural stimulationsignal to the IVC-LA fat pad during AVCVT event to block AV conductionto terminate the AVCVT event, and provide bradycardia support pacingwhen the neural stimulation signal is applied to the IVC-LA fat pad.

In various embodiments, the device includes a header, a right atriumdetector, a right ventricle detector, a neural stimulator and a cardiacpacing stimulator. The header includes a first port to connect to afirst lead with at least one electrode to be located to sense intrinsicsignals from a right atrium, a second port to connect to a second leadwith at least one electrode to be located to sense intrinsic signalsfrom and provide electrical stimulation to a right ventricle, and atleast a third port to connect to at least a third lead to beintravascularly inserted through a coronary sinus with at least oneelectrode located to sense intrinsic signals from and provide electricalstimulation to a left ventricle and at least one electrode located tostimulate an IVC-LA fat pad. The right atrium detector is connected tothe first port of the header to sense an atrial rate based on intrinsicsignals from the right atrium for use in determining an AV-ConductedVentricular Tachyarrhythmia (AVCVT) event. The right ventricle detectoris connected to the second port of the header to sense a ventricularrate based on intrinsic signals from the right ventricle for use indetermining the AVCVT event. The neural stimulator is connected to theat least one third port of the header to selectively apply a neuralstimulation signal to the IVC-LA fat pad during the AVCVT event to slowAV conduction and terminate the AVCVT event. The cardiac pacingstimulator is connected to the second port and the at least one thirdport to provide bradycardia support pacing to maintain at least aprogrammable minimum heart rate when the neural stimulation signal isapplied to the IVC-LA fat pad and to provide biventricular pacing aspart of a cardiac resynchronization therapy.

Various aspects of the present subject matter relate to a method totreat to treat AV-conducted ventricular tachyarrhythmia (AVCVT).According to various embodiments of the method, an AVCVT is sensed, anIVC-LA fat pad is stimulated when the AVCVT is sensed to block AVconduction, and bradycardia support pacing is provided while the IVC-LAfat pad is stimulated.

This Summary is an overview of some of the teachings of the presentapplication and not intended to be an exclusive or exhaustive treatmentof the present subject matter. Further details about the present subjectmatter are found in the detailed description and appended claims. Otheraspects will be apparent to persons skilled in the art upon reading andunderstanding the following detailed description and viewing thedrawings that form a part thereof, each of which are not to be taken ina limiting sense. The scope of the present invention is defined by theappended claims and their equivalents.

BRIEF DESCRIPTION OF THE DRAWINGS

FIGS. 1A-1C illustrate a heart and are useful to illustrate thephysiology associated with the electrical stimulation of the IVC-LA fatpad to selectively block AV conduction and terminate AV-conductedventricular tachyarrhythmia (AVCVT) according to embodiments of thepresent subject matter.

FIGS. 2A and 2B illustrate various embodiments of an implantable medicaldevice and lead positions used to detect an AVCVT induced by an SVT,apply neural stimulation to the IVC-LA fat pad to selectively andtemporarily block the AV conduction during the SVT to terminate and/orprevent the AVCVT, and provide bradycardia support pacing when theneural stimulation is applied and the AV conduction is inhibited.

FIG. 3 illustrates a system diagram of an implantable medical deviceconfigured for multi-site stimulation and sensing.

FIGS. 4A and 4B schematically illustrates various embodiments of animplantable medical device used to detect an AVCVT, apply neuralstimulation to the IVC-LA fat pad to selectively block the AV conductionand terminate the AVCVT, and provide bradycardia support pacing when theneural stimulation is applied.

FIG. 5 schematically illustrates an embodiment of a neural stimulator,such as can be implemented at 473 FIGS. 4A and 4B.

FIG. 6 schematically illustrates logic associated with a SVT detector,such as can be implemented as generally illustrated at 471A in FIGS. 4Aand 4B, and further illustrates logic associated with a SVT detector,such as can be implemented as generally illustrated at 471B in FIGS. 4Aand 4B, according to various embodiments of the present subject matter.

FIG. 7 schematically illustrates logic associated with a bradycardiasupport pacing circuit, such as can be implemented at 472 in FIGS. 4Aand 4B, according to various embodiments of the present subject matter.

FIG. 8 illustrates a method to treat AVCVT, according to variousembodiments of the present subject matter.

DETAILED DESCRIPTION

The following detailed description of the present subject matter refersto the accompanying drawings which show, by way of illustration,specific aspects and embodiments in which the present subject matter maybe practiced. These embodiments are described in sufficient detail toenable those skilled in the art to practice the present subject matter.Other embodiments may be utilized and structural, logical, andelectrical changes may be made without departing from the scope of thepresent subject matter. References to “an”, “one”, or “various”embodiments in this disclosure are not necessarily to the sameembodiment, and such references contemplate more than one embodiment.The following detailed description is, therefore, not to be taken in alimiting sense, and the scope is defined only by the appended claims,along with the full scope of legal equivalents to which such claims areentitled.

The following disclosure refers to paroxysmal atrial tachycardia (PAT)and AV nodal reentry tachycardia (AVNRT) as an example of SVT. Those ofordinary skill in the art will understand, upon reading andcomprehending this disclosure, how to treat AV-conducted ventriculartachyarrhythmia (AVCVT) associated with a variety of SVTs.

Cardiac Physiology

FIGS. 1A-1C illustrate a heart and are useful to illustrate thephysiology associated with the electrical stimulation of the IVC-LA fatpad to selectively block AV conduction and terminate AVCVT according toembodiments of the present subject matter. The illustrated heart 100includes a right atrium 102, a right ventricle 104, a left atrium 106and a left ventricle 108. The illustrated heart 100 also includes asinoatrial (SA) node 110 and an atrioventricular (AV) node 112. FIG. 1Aillustrates the cardiac conduction system which controls heart rate.This system generates electrical impulses and conducts them throughoutthe muscle of the heart to stimulate the heart to contract and pumpblood. The cardiac conduction system includes the SA node 110 and the AVnode 112. The autonomic nervous system controls the firing of the SAnode to trigger the start of the cardiac cycle. The SA node includes acluster of cells in the right atrium that generates the electricalimpulses. The electrical signal generated by the SA node moves from cellto cell down through the heart until it reaches the AV node 112, acluster of cells situated in the center of the heart between the atriaand ventricles. The AV node functions as an electrical relay stationbetween the atria and the ventricles, such that electrical signals fromthe atria must pass through the AV node to reach the ventricles. The AVnode slows the electrical current before the signal is permitted to passdown through to the ventricles, such that the atria are able to fullycontract before the ventricles are stimulated. After passing the AVnode, the electrical current travels to the ventricles along specialfibers 114 embedded in the walls of the lower part of the heart.

The nervous system regulating the rhythm of the heart includes a numberof ganglionated fat pads, including a fat pad associated with the SAnode and a fat pad associated with the AV node. Stimulation of the fatpad associated with the SA node results in slowing of the sinus ratewithout prolonging AV conduction time, and stimulation of the fat padassociated with the AV node extends the AV conduction time withoutslowing of the sinus rate. Embodiments of the present subject matterselectively stimulate the fat pad associated with the AV node to providean AV conduction block. The AV conduction block is reversible, as itexists for a time period corresponding to the time that the fat pad isstimulated.

FIGS. 1B and 1C illustrate other views a heart, including an IVC-LA fatpad 116 (a fat pad located between the inferior vena cava and the leftatrium) that is electrically stimulated to selectively block the AVconduction according to embodiments of the present subject matter. FIGS.1B and 1C illustrate the right side and left side of the heart,respectively. FIG. 1B illustrates the right atrium 102, right ventricle104, SA node 110, superior vena cava 118, inferior vena cava 120, aorta122, right pulmonary veins 124, and right pulmonary artery 126. FIG. 1Balso illustrates a cardiac fat pad 128 between the superior vena cavaand aorta. FIG. 1C illustrates the left atrium 106, left ventricle 108,right atrium 102, right ventricle 104, superior vena cava 118, inferiorvena cava 120, aorta 122, right pulmonary veins 130, left pulmonary vein132, right pulmonary artery 134, and coronary sinus 136. FIG. 1C alsoillustrates a cardiac fat pad 138 located proximate to the right cardiacveins and a cardiac fat pad 116 (also referred to herein as the IVC-LAfat pad) located proximate to or at the junction of the inferior venacava and left atrium. Nerve endings in the IVC-LA fat pad 116 arestimulated in some embodiments using an electrode screwed into the fatpad using either an epicardial or intravascular lead, and aretransvascularly stimulated in some embodiments using an intravascularelectrode proximately positioned to the fat pad in a vessel such as theinferior vena cava 120 or coronary sinus 136 or a lead in the leftatrium 106, for example.

Treatment of AV-Conducted Ventricular Tachyarrhythmia

Previously published data indicate that a 10V, 30 Hz, 0.05 ms bipolarelectrical stimulation of the IVC-LA fat pad results in a selectiveincrease in AV conduction time with minimal effects of sinus cyclelength and atrial contractility. The present subject matter effectivelyturns conduction through the AV node off and on at will by selectivelystimulating the IVC-LA fat pad. The present subject matter provides atreatment of AV-conducted ventricular tachyarrhythmia (AVCVT) thatincludes stimulating autonomic ganglia in the fat pad associated withthe AV node to selectively block conduction through the AV node andprevent fast ventricular rates associated with SVTs. Embodiments of thepresent subject matter sense an AVCVT induced by an SVT such as a PAT.In response, electrical stimulus is selectively delivered to the IVC-LAfat pad to selectively block AV conduction. Embodiments of the presentsubject matter sense an atrial tachycardia event (e.g. an atrial rate ofapproximately 160-200 bpm), and selectively stimulate the IVC-LA fat padto selectively block AV conduction time to terminate the AVCVT. Thedelivery of the electrical stimulus to the IVC-LA fat pad is controlledto continue the AV conduction block until the triggering SVT stops and anormal sinus rhythm (NSR) is sensed. A triggering SVT can revert to aNSR on its own. A triggering AVNRT can be terminated by the AVconduction block provided by the neural stimulation of the autonomicganglia in the AV-LA fat pad. Ventricular rate support is providedduring the AV-conduction block to maintain an appropriate ventricularrhythm.

In an embodiment, when a PAT is sensed, the IVC-LA fat pad iselectrically stimulated at a magnitude determined by closed-loop controlusing sensed cardiac intrinsic signals to terminate the PAT. In variousembodiments, a pacemaker supports the ventricular rate by appropriatelypacing the right ventricle when the AV conduction is inhibited. Afterthe device detects that the atrial tachyarrhythmia has terminated, theelectrical stimulation of the IVC-LA fat pad stops, thus providing aclosed loop pacing system.

Various implantable device embodiments are used solely to terminate theAVCVT. These embodiments can use a relatively small battery to power thedevice because the stimulation is provided only during episodes ofatrial tachycardia or other SVT that induced ventricular arrhythmia viaconduction through the AV node. Various embodiments of the presentsubject matter use a pacemaker with an implantable stimulation electrodeto selectively stimulate the nerves at the IVC-LA fat pad. In variousembodiments, the electrode is placed on the epicardial surface of theheart at the IVC-LA fat pad. In various embodiments, the electrode ispositioned within the coronary sinus to transvascularly stimulate theIVC-LA fat as part of a complete percutaneous implant. Thus, incomparison to defibrillation shocks and surgical ablation, the presentsubject matter provides a less invasive and effective treatment for PAT.Furthermore, with respect to AV surgical ablation, the present subjectmatter provides a temporary and reversible AV block. Thus, the presentsubject matter is well-suited to treat temporary arrhythmic episodeswith a temporary AV block. Additionally, stimulating the IVC-LA fat padrather than a vagus nerve trunk selectively provides the AV blockwithout causing other unintended consequences that can occur if thevagus nerve trunk is stimulated.

Device Embodiments and Lead Positions

FIGS. 2A and 2B illustrate various embodiments of an implantable medicaldevice and lead positions used to detect an AVCVT induced by an SVT,apply neural stimulation to the IVC-LA fat pad to selectively andtemporarily block the AV conduction during the SVT to terminate and/orprevent the AVCVT, and provide bradycardia support pacing when theneural stimulation is applied and the AV conduction is inhibited.

In FIG. 2A, the illustrated implantable medical device 240A has threeleads. A first lead 242 is placed in or proximate to the right atrium todetect intrinsic signals indicative of an atrial rate, which is capableof being used to determine a SVT event such as a PAT event. A secondlead 244 is placed in or proximate to the right ventricle to pace theright ventricle, and detect intrinsic signals indicative of ventricularrate, which is capable of being used to determine AVCVT. The third lead246A is placed proximate to the IVC-LA fat pad 216 to apply neuralstimulation to the IVC-LA fat pad. Various embodiments use epicardialleads; various embodiments use intravascularly-fed leads; and variousembodiments use various combinations of epicardial andintravascularly-fed leads. Thus, in an embodiment, the first, second andthird leads are intravascularly inserted through a peripheral vein intothe right atrium, and the first lead terminates therein. The second leadcontinues from the right atrium through the tricuspid valve into theright ventricle of the heart and terminates therein at a position topace the right ventricle. The third lead enters the coronary sinus tointravascularly place an electrode therein and transvascularly stimulatethe IVC-LA fat pad.

FIG. 2B is similar to FIG. 2A. However, in FIG. 2B, the third lead 246Bfor the device 240B extends further into the coronary sinus to place anelectrode to pace the left ventricle. In various embodiments, one lead,such as the illustrated third lead, is used to stimulate the IVC-LA fatpad and to pace the left ventricle. In various embodiments, one lead isinserted into the coronary sinus to stimulate the IVC-LA fat pad and asecond lead is used to pace the left ventricle. Such a system as isillustrated in FIG. 2B can be used to provide cardiac resynchronizationtherapy (CRT), which is discussed below.

Implantable cardiac devices that provide electrical stimulation toselected chambers of the heart have been developed in order to treat anumber of cardiac disorders. A pacemaker, for example, is a device whichpaces the heart with timed pacing pulses, most commonly for thetreatment of bradycardia where the ventricular rate is too slow. AVconduction defects (i.e., AV block) and sick sinus syndrome representthe most common causes of bradycardia for which permanent pacing may beindicated. If functioning properly, the pacemaker makes up for theheart's inability to pace itself at an appropriate rhythm in order tomeet metabolic demand by enforcing a minimum heart rate. Implantabledevices may also be used to treat cardiac rhythms that are too fast,with either anti-tachycardia pacing or the delivery of electrical shocksto terminate fibrillation.

Implantable devices have also been developed that affect the manner anddegree to which the heart chambers contract during a cardiac cycle inorder to promote the efficient pumping of blood. The heart pumps moreeffectively when the chambers contract in a coordinated manner, a resultnormally provided by the specialized conduction pathways in both theatria and the ventricles that enable the rapid conduction of excitation(i.e., depolarization) throughout the myocardium. These pathways conductexcitatory impulses from the SA node to the atrial myocardium, to the AVnode, and thence to the ventricular myocardium to result in acoordinated contraction of both atria and both ventricles. This bothsynchronizes the contractions of the muscle fibers of each chamber andsynchronizes the contraction of each atrium or ventricle with thecontralateral atrium or ventricle. Without the synchronization affordedby the normally functioning specialized conduction pathways, the heart'spumping efficiency is greatly diminished. Pathology of these conductionpathways and other inter-ventricular or intra-ventricular conductiondeficits can be a causative factor in heart failure, which refers to aclinical syndrome in which an abnormality of cardiac function causescardiac output to fall below a level adequate to meet the metabolicdemand of peripheral tissues. In order to treat these problems,implantable cardiac devices have been developed that provideappropriately timed electrical stimulation to one or more heart chambersin an attempt to improve the coordination of atrial and/or ventricularcontractions, termed cardiac resynchronization therapy (CRT).Ventricular resynchronization is useful in treating heart failurebecause, although not directly inotropic, resynchronization can resultin a more coordinated contraction of the ventricles with improvedpumping efficiency and increased cardiac output. Currently, a commonform of CRT applies stimulation pulses to both ventricles, eithersimultaneously or separated by a specified biventricular offsetinterval, and after a specified AV delay interval with respect to thedetection of an intrinsic atrial contraction or delivery of an atrialpace.

Implantable Medical Device

FIG. 3 illustrates a system diagram of an implantable medical deviceembodiment configured for multi-site stimulation and sensing. Threeexemplary sensing and pacing channels designated “A” through “C”comprise bipolar leads with ring electrodes 250A-C and tip electrodes251A-C, sensing amplifiers 252A-C, pulse generators 253A-C, and channelinterfaces 254A-C. Each channel thus includes a pacing channel made upof the pulse generator connected to the electrode and a sensing channelmade up of the sense amplifier connected to the electrode. The channelinterfaces 254A-C communicate bidirectionally with microprocessor 255,and each interface may include analog-to-digital converters fordigitizing sensing signal inputs from the sensing amplifiers andregisters that can be written to by the microprocessor in order tooutput pacing pulses, change the pacing pulse amplitude, and adjust thegain and threshold values for the sensing amplifiers. The sensingcircuitry of the pacemaker detects a chamber sense, either an atrialsense or ventricular sense, when an electrogram signal (i.e., a voltagesensed by an electrode representing cardiac electrical activity)generated by a particular channel exceeds a specified detectionthreshold. Pacing algorithms used in particular pacing modes employ suchsenses to trigger or inhibit pacing, and the intrinsic atrial and/orventricular rates can be detected by measuring the time intervalsbetween atrial and ventricular senses, respectively.

The switching network 256 is used to switch the electrodes to the inputof a sense amplifier in order to detect intrinsic cardiac activity andto the output of a pulse generator in order to deliver a pacing pulse.The switching network also enables the device to sense or pace either ina bipolar mode using both the ring and tip electrodes of a lead or in aunipolar mode using only one of the electrodes of the lead with thedevice housing or can 257 serving as a ground electrode or anotherelectrode on another lead serving as the ground electrode. A shock pulsegenerator 258 is also interfaced to the controller for delivering adefibrillation shock via a pair of shock electrodes 259 to the atria orventricles upon detection of a shockable tachyarrhythmia.

The controller or microprocessor controls the overall operation of thedevice in accordance with programmed instructions stored in memory 260,including controlling the delivery of paces via the pacing channels,interpreting sense signals received from the sensing channels, andimplementing timers for defining escape intervals and sensory refractoryperiods. The controller is able to determine refractory periods for bothintrinsic events and paced events. The controller is capable ofoperating the device in a number of programmed pacing modes which definehow pulses are output in response to sensed events and expiration oftime intervals. Most pacemakers for treating bradycardia are programmedto operate synchronously in a so-called demand mode where sensed cardiacevents occurring within a defined interval either trigger or inhibit apacing pulse. Inhibited demand pacing modes utilize escape intervals tocontrol pacing in accordance with sensed intrinsic activity such that apacing pulse is delivered to a heart chamber during a cardiac cycle onlyafter expiration of a defined escape interval during which no intrinsicbeat by the chamber is detected. Escape intervals for ventricular pacingcan be restarted by ventricular or atrial events, the latter allowingthe pacing to track intrinsic atrial beats. CRT is most convenientlydelivered in conjunction with a bradycardia pacing mode where, forexample, multiple excitatory stimulation pulses are delivered tomultiple sites during a cardiac cycle in order to both pace the heart inaccordance with a bradycardia mode and provide pre-excitation ofselected sites. A telemetry interface 261 is also provided which enablesthe controller to communicate with an external programmer or remotemonitor. According to embodiments of the present subject matter, theimplantable medical device tracks the atrial rate, switching modes uponthe occurrence of a SVT to block AV conduction and provide bradycardialife support pacing to the ventricle.

Neural stimulation channels are incorporated into the device fordelivering neural stimulation to the IVC-LA fat pad, where one channelincludes a bipolar lead with a ring electrode 262 and a tip electrode263, a pulse generator 264, and a channel interface 265. Otherembodiments may use unipolar leads in which case the neural stimulationpulses are referenced to the can or another electrode. The pulsegenerator for each channel outputs a train of neural stimulation pulseswhich may be varied by the controller as to amplitude, frequency, andduty-cycle. Some embodiments time the delivery of the neural stimulationto the IVC-LA fat pad with a ventricular refractory period (either asensed intrinsic or paced ventricular beat) to avoid collateralstimulation of the myocardium. The delivery of the neural stimulationcan be controlled (reduced or terminated) based on the ventricularrefractory period to avoid capturing ventricular tissue with the neuralstimulation.

FIGS. 4A and 4B schematically illustrates various embodiments of animplantable medical device used to detect an AVCVT, apply neuralstimulation to the IVC-LA fat pad to selectively block the AV conductionand terminate the AVCVT, and provide bradycardia support pacing when theneural stimulation is applied. The illustrated medical devices of FIGS.4A-4B include pacing and sensing channels, as generally illustrated inFIG. 3, but are illustrated with functional blocks to further illustratethe present subject matter.

FIG. 4A illustrates an implantable medical device, such as can be usedfor the devices illustrated in FIGS. 2A and 2B. The illustrated device440 includes a pulse generator 466 and a header 467. The header 467includes at least one port 468 to receive at least one lead 469 that hasat least one electrode. The header 467 functions as an interface betweenthe lead(s) 469 and the pulse generator 466. The illustrated pulsegenerator includes a controller 470 connected to a memory 460 and atelemetry interface 461 to communicate with an external programmer. Thecontroller 470 is connected to a sensing circuit 471A that functions asa SVT detector (a detector capable of detecting an SVT event such asPAT, AT, AF that induced VT through AV conduction), a sensing circuit471B that functions as a ventricular rate detector, a cardiac stimulator472 that cooperates with the ventricular rate sensing circuit 471B andfunctions as a bradycardia support pacer, and a neural stimulatingcircuit 473 that functions as an IVC-LA fat pad neural stimulator.

In various embodiments, a VT detector 471B provides ventricular ratefeedback. The ventricular rate feedback can be used to provide closedloop control of the neural stimulation to the IVC-LA fat pad. The VTdetector 471B in cooperation with the detector 471A is able to detectwhen a VT is triggered by an SVT event through AV conduction. Forexample, the SVT detector 471B is used to titrate the neural stimulationtherapy to block the AV conduction. If the intrinsic ventricular ratefalls below the minimum threshold such as occurs during an AV block, thebradycardia support pacing circuit 472 provides demand pacing tomaintain at least the minimum threshold for the ventricular rate.

In some embodiments where it is determined that the applied neuralstimulation is capable of capturing ventricular tissue, the controller470, neural stimulating circuit 473, bradycardia support pacing circuit472 and sensing circuit 471B cooperate with each other to determine whena ventricular refractory period is occurring, and to time the deliveryof the neural stimulation to block the AV conduction during therefractory period. The controller 470 and neural stimulating circuit 473cooperate to apply neural stimulation to selectively gate the AVconduction. According to these embodiments, when the controller 470 andsensing circuit 471B determine the refractory period is complete oralmost complete, the controller 470 and neural stimulating circuit 473cooperate to temporarily reduce or terminate the neural stimulation toprevent capturing ventricular tissue. The reduced or terminated neuralstimulation increases conduction through the AV node. If an intrinsicventricular event is detected during the time without the AV conductionblock, neural stimulation is again applied during the subsequentrefractory period. Else, a ventricular pace is provided after an escapeinterval as part of the bradycardia support pacing therapy, and neuralstimulation is applied during the subsequent refractory period.

The SVT detector (e.g. PAT sensor), VT detector, bradycardia supportpacer and IVC-LA fat pad neural stimulator appropriately interface withthe electrode(s) on the lead(s) via switches 456 (e.g. MOS switches).The switches provide logical connections that allow circuits 471A, 471B,472, and 473 to connect to a desired port 468 to access a desiredelectrode channel on a desired lead. FIG. 4A illustrates circuits 471A,471B, 472, and 473 as being distinct from controller 470. As will beunderstood by those of ordinary skill in the art upon reading andcomprehending this disclosure, various functions associated withcircuits 471A, 471B, 472, and 473 can be integrated with controller 470in various embodiments. The controller 470 is adapted to determine anSVT (e.g. PAT) event from an intrinsic signal sensed by the SVT detector471A, apply the neural stimulation signal to the IVC-LA fat pad duringSVT event using the neural stimulator 473 to block AV conduction andduring the SVT event to terminate the AVCVT, and provide bradycardiasupport pacing using the cardiac stimulator 472 when the neuralstimulation signal is applied to the IVC-LA fat pad. Blocking the AVconduction can also serve to terminate AVNRT/PAT.

FIG. 4B illustrates an implantable medical device 440 such as can beused for the device illustrated in FIG. 2B to treat PAT and to provideCRT. For the sake of clarity, FIG. 4B illustrates connections betweencircuits 471A, 471B, 472, and 473 to ports 468A, 468B and 468C. A switch(SW) is generally illustrated proximate to the bradycardia supportpacing circuit 472. The illustrated switch is capable of providing thedesired connections, and disconnects, between the circuits 471B and 472and the ports 468B and 468C to perform the functions provided below.FIG. 4B illustrates a CRT module 474, which includes sensing andstimulating capabilities. In the illustrated embodiment, the CRT moduleincludes a right atrium sensor 471A for use in determining PAT or otherSVT, a right ventricular sensor to detect ventricular rate to determineAVCVT triggered by PAT or other SVT, and a bradycardia support pacer 472used in conjunction with the right ventricular sensor to provide supportpacing. According to various embodiments, the PAT detector andbradycardia support pacer are integrated with the sensors andstimulators used by the CRT module.

In the illustrated embodiment, the right atrium sensor/detector 471A islogically connected to a right atrium port 468A to receive a rightatrium lead 469A to be placed in the right atrium. The right atriumsensor/detector is adapted to determine an atrial rate from an intrinsicsignal received by an electrode on the right atrium lead. The atrialrate is used to determine if a SVT event has taken place. The rightventricle sensor/detector 471B is logically connected to a rightventricle port 468B to receive a right ventricle lead 469B to be placedin the right ventricle. The right ventricle sensor/detector is adaptedto determine a ventricular rate from an intrinsic signal received by anelectrode on the right ventricle lead. Some embodiments compare theventricular rate to the atrial rate to verify that a ventriculartachyarrhythmia is attributable to an SVT conducted through the AV node.In various embodiments, the ventricular rate is used to provideclosed-loop control of the neural stimulating circuit to block AVconduction, and further is used to provide feedback to pace the rightventricle as part of bradycardia support pacing. FIG. 4B illustrates thebradycardia support pacer 472 connected to both a right ventricle port468B and at least one coronary sinus port 468C, and further illustratesthe IVC-LA fat pad neural stimulator 473 connected to the coronary sinusport(s) 468C. The right ventricle port 468B is adapted to receive a lead469B with at least one electrode to sense and pace the right ventricle.The coronary sinus port(s) 468C is adapted to receive at least one lead469C with at least one electrode to be fed through the coronary sinus,to apply a neural stimulation signal to the IVC-LA fat pad and to senseand pace the left ventricle. Various embodiments include one coronarysinus port to receive one lead to be intravascularly fed into thecoronary sinus; and various embodiments include two coronary sinus portsto receive one lead intravascularly fed into the coronary sinus for useto apply a neural stimulation signal to the IVC-LA fat pad and anotherlead intravascularly fed into the coronary sinus for use to sense andpace the left ventricle.

FIG. 5 schematically illustrates an embodiment of a neural stimulator573, such as can be implemented at 473 in FIGS. 4A and 4B. Theillustrated neural stimulator embodiment is adapted to adjust theintensity of the applied neural stimulation to the IVC-LA node tofurther inhibit AV node conduction if appropriate to AVCVT, and in someembodiments to terminate AVNRT. Thus, for example, if a 10 V, 30 Hz, 0.5ms neural stimulation signal is unsuccessful in terminating the SVT, theneural stimulation signal is adjusted. Various embodiments adjust theamplitude of the signal to increase the neural stimulation and furtherinhibit the AV node conduction. Various embodiments adjust the frequencyof the signal to increase the neural stimulation and further inhibit theAV node conduction. Various embodiments adjust the burst frequency ofthe signal to increase the neural stimulation and further inhibit the AVnode conduction. Various embodiments adjust the wave morphology (e.g.triangular, sinusoidal, square, white noise) of the signal to increasethe neural stimulation and further inhibit the AV node conduction.Various embodiments adjust a combination of two or more of theamplitude, the frequency, the burst frequency and the wave morphology ofthe signal to increase the neural stimulation and further inhibit the AVnode conduction. Functions associated with the neural stimulator can beintegrated with the controller.

FIG. 6 schematically illustrates logic associated with a SVT detector,such as can be implemented as generally illustrated at 471A in FIGS. 4Aand 4B, and further illustrates logic associated with a SVT detector,such as can be implemented as generally illustrated at 471B in FIGS. 4Aand 4B, according to various embodiments of the present subject matter.

Embodiments of the present subject matter are able to selectively turnoff and on AV conduction through the selective stimulation of autonomicganglia in the IVC-LA fat pad. Some embodiments deliver the neuralstimulation to the fat pad epicardially, and some embodiments deliverthe neural stimulation to the fat pad using transvascular stimulation.

The illustrated PAT detector 671A includes atrial rate detector 675, aventricular rate detector, and a memory or register 676 for use to storea value corresponding to a programmable PAT atrial rate threshold. Theillustrated detector compares the detected atrial rate to the storedthreshold value and to the detected ventricular rate, and provides anindication 677 of a PAT event based on the comparison if the rate ishigher than the threshold and if the ventricular rate is following theatrial rate, which indicates AVCVT. In various embodiments, the PATatrial rate threshold is within a range of 160 to 200 beats per minute.Functions associated with the PAT detector can be integrated with thecontroller.

The illustrated VT detector 671B includes a ventricular rate detector690 and further includes a memory or register 691 for use to store avalue corresponding to a programmable VT threshold. The illustrated VTdetector compares the detected ventricular rate to the stored thresholdvalue, and provides an indication of a VT event based on the comparison.Functions associated with the VT detector can be integrated with thecontroller. In various embodiments, the VT detector and SVT/PAT detectorare integrated such that intrinsic signals are sensed from both theright atrium and the right ventricle to determine an occurrence of a PATevent and to determine the efficacy of the neural stimulation therapy.The figure illustrates the ventricular rate detector 696 shared by theSVT/PAT detector 671A and the VT detector 671B.

FIG. 7 schematically illustrates logic associated with a bradycardiasupport pacing circuit 772, such as can be implemented at 472 in FIGS.4A and 4B, according to various embodiments of the present subjectmatter. The illustrated circuit includes an intrinsic event or eventssensor 778, and further includes a memory or register 779 for use tostore a value corresponding to a programmable minimum ventricular heartrate or escape interval. The illustrated circuit compares the sensedventricular rate to the programmable minimum rate or escape interval toprovide an indicator 780 to apply a pacing pulse. Functions associatedwith the bradycardia support pacing circuit can be integrated with thecontroller.

FIG. 8 illustrates a method to treat AV-Conducted VentricularTachyarrhythmias (AVCVT), according to various embodiments of thepresent subject matter. The illustrated method is capable of beingstored as computer-readable instructions in memory 460 and executed bycontroller 470 using circuits 471, 472 and 473 in FIGS. 4A-4B, forexample. At 881, it is determined if a PAT event (or other AVCVT event)is occurring. If a PAT event is occurring, the process proceeds to 882to provide neural stimulation to the IVC-LA fat pad and to 883 toprovide bradycardia support pacing during the AV conduction block thatoccurs while the IVC-LA fat pad is being stimulated. Some embodimentscontrol delivery of the neural stimulation based on ventricularrefractory period to avoid capturing ventricular tissue with the neuralstimulation. The ventricular refractory period can be caused by anintrinsic beat or a ventricular pace. According to various embodiments,it is determined at 884 whether the VT associated with the PAT has beenterminated. If the VT has not been terminated, the process proceeds to885 to adjust the neural stimulation therapy (e.g. amplitude, frequency,burst frequency, and/or wave morphology), and returns to 882 to provideneural stimulation to the IVC-LA fat pad and to 883 to providebradycardia support pacing during the AV conduction inhibition thatoccurs while the IVC-LA fat pad is being stimulated. If the VT hasterminated, the process proceeds from 884 to 886 to determine if the PAThas ended. The PAT may revert on its own. For AVNRT, the PAT may endbased on the neural stimulation, which slows conduction through afeedback path passing through the AV node. If the PAT has not ended, theprocess proceeds from 886 back to 884 to determine if the VT has beenterminated. If the PAT has ended, the process proceeds from 886 to 887to end the neural stimulation and support pacing, and returns to 881 todetermine if a PAT has occurred.

One of ordinary skill in the art will understand that, the modules andother circuitry shown and described herein can be implemented usingsoftware, hardware, and combinations of software and hardware. As such,the term module is intended to encompass software implementations,hardware implementations, and software and hardware implementations.

The methods illustrated in this disclosure are not intended to beexclusive of other methods within the scope of the present subjectmatter. Those of ordinary skill in the art will understand, upon readingand comprehending this disclosure, other methods within the scope of thepresent subject matter. The above-identified embodiments, and portionsof the illustrated embodiments, are not necessarily mutually exclusive.These embodiments, or portions thereof, can be combined. In variousembodiments, the methods provided above are implemented as a computerdata signal embodied in a carrier wave or propagated signal, thatrepresents a sequence of instructions which, when executed by aprocessor cause the processor to perform the respective method. Invarious embodiments, methods provided above are implemented as a set ofinstructions contained on a computer-accessible medium capable ofdirecting a processor to perform the respective method. In variousembodiments, the medium is a magnetic medium, an electronic medium, oran optical medium.

Although specific embodiments have been illustrated and describedherein, it will be appreciated by those of ordinary skill in the artthat any arrangement which is calculated to achieve the same purpose maybe substituted for the specific embodiment shown. This application isintended to cover adaptations or variations of the present subjectmatter. It is to be understood that the above description is intended tobe illustrative, and not restrictive. Combinations of the aboveembodiments as well as combinations of portions of the above embodimentsin other embodiments will be apparent to those of skill in the art uponreviewing the above description. The scope of the present subject mattershould be determined with reference to the appended claims, along withthe full scope of equivalents to which such claims are entitled.

1. An implantable device, comprising: means for sensing an atrial tachyarrhythmia; means for stimulating an IVC-LA fat pad located between an inferior vena cava and a left atrium in response to a sensed atrial tachyarrhythmia to block AV conduction and terminate AV-Conducted Ventricular Tachyarrhythmia (AVCVT); and means for providing bradycardia support pacing when the IVC-LA fat pad is stimulated.
 2. The device of claim 1, wherein the means for sensing an atrial tachycardia includes means for sensing a heart rate and identifying when the heart rate exceeds a threshold value.
 3. The device of claim 1, wherein the means for stimulating an IVC-LA fat pad includes an intravascular lead adapted to be fed into a coronary sinus.
 4. The device of claim 3, wherein the intravascular lead includes an intravascular bipolar electrode to transvascularly stimulate the IVC-LA fat pad from the coronary sinus.
 5. The device of claim 3, wherein the intravascular lead includes a bipolar electrode to pierce through the coronary sinus and be fixed in the IVC-LA fat pad.
 6. The device of claim 3, wherein the means for stimulating an IVC-LA fat pad includes an epicardial lead with a bipolar electrode adapted to be fixed to the IVC-LA fat pad.
 7. A method to treat AV-Conducted Ventricular Tachyarrhythmia (AVCVT), comprising: sensing an AVCVT; stimulating an IVC-LA fat pad when the AVCVT is sensed to selectively block AV conduction; and providing bradycardia support pacing while the IVC-LA fat pad is stimulated.
 8. The method of claim 7, wherein stimulating an IVC-LA fat pad includes applying a neural stimulation signal having a magnitude of approximately 10 Volts, a frequency of approximately 30 Hz, and a duration of approximately 0.05 ms.
 9. The method of claim 7, wherein sensing an AVCVT includes sensing a heart rate and declaring an AVCVT event when the heart rate is above a threshold.
 10. The method of claim 7, wherein sensing an AVCVT includes sensing a right atrial rate and declaring an AVCVT event when the right atrial rate is above a threshold.
 11. The method of claim 7, wherein sensing an AVCVT includes: sensing a right atrial rate; sensing a right ventricular rate; declaring an AVCVT event when the right ventricular rate is above a threshold and the right ventricular rate tracks with the right atrial rate.
 12. The method of claim 7, wherein stimulating an IVC-LA fat pad includes stimulating the IVC-LA fat pad through an epicardial lead with an electrode fixed to the IVC-LA fat pad.
 13. The method of claim 7, wherein stimulating an IVC-LA fat pad includes stimulating the IVC-LA fat pad through an intravascular lead in a coronary sinus with an electrode pierced through the coronary sinus and fixed to the IVC-LA fat pad.
 14. The method of claim 7, wherein stimulating an IVC-LA fat pad includes stimulating the IVC-LA fat pad through an intravascular lead in a coronary sinus with an intravascular bipolar electrode to transvascularly stimulate the IVC-LA fat pad from the coronary sinus.
 15. The method of claim 7, wherein stimulating an IVC-LA fat pad includes increasing a stimulation intensity to the IVC-LA fat pad if the AVCVT is not terminated after an initial stimulation of the IVC-LA fat pad.
 16. The method of claim 15, wherein increasing a stimulation intensity includes adjusting an amplitude of a neural stimulation signal applied to the IVC-LA fat pad.
 17. The method of claim 15, wherein increasing a stimulation intensity includes adjusting a frequency of a neural stimulation signal applied to the IVC-LA fat pad.
 18. The method of claim 15, wherein increasing a stimulation intensity includes adjusting a burst frequency of a neural stimulation signal applied to the IVC-LA fat pad.
 19. The method of claim 15, wherein increasing a stimulation intensity includes adjusting a wave morphology of a neural stimulation signal applied to the IVC-LA fat pad.
 20. The method of claim 7, wherein the AVCVT includes a PAT event, and stimulating an IVC-LA fat pad terminates the AVCVT and the PAT event.
 21. The method of claim 7, wherein stimulating an IVC-LA fat pad includes identifying a ventricular refractory period and controlling delivery of the neural stimulation based on the ventricular refractory period to avoid capturing ventricular tissue with the neural stimulation. 